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Oral SCC (oral + scc)
Selected AbstractsEffectiveness of routine follow-up of patients treated for T1,2N0 oral squamous cell carcinomas of the floor of mouth and tongueHEAD & NECK: JOURNAL FOR THE SCIENCES & SPECIALTIES OF THE HEAD AND NECK, Issue 1 2006Matthias Adrianus Wilhelmus Merkx MD Abstract Background. The duration of follow-up after treatment for head and neck cancer, the depth of the routine visits, and the diagnostic tools used are determined on the basis of common acceptance rather than evidence-based practice. Patients with early-stage tumors are more likely to benefit from follow-up programs, because they have the best chance for a second curative treatment after recurrence. The purpose of this study was to determine the benefit of our 10-year follow-up program in patients with stage I and II squamous cell carcinoma (SCC) of the floor of mouth and tongue. Methods. In a longitudinal cohort study involving 102 patients who were treated with curative intent for a pT1,2N0M0 SCC of the floor of mouth and tongue from 1989,1998 with a minimum follow-up of 5 years, we evaluated the effect of routine follow-up. Results. During the follow-up (mean, 61 months; SD, 4 months), 10 patients had a recurrence, and 20 patients had a second primary tumor. No regional lymph node recurrences in the neck were detected. Location, T classification of the primary tumor, choice of therapy, or measure of tumor-free margins in the resection did not significantly affect the occurrence of a secondary event (p , .1). The secondary event was discovered during a patient-initiated visit for complaints in 14 patients and was found during routine follow-up visits in 16 patients. Only seven second primary tumors were detected after 60 months, four on routine follow-up and three on a self-initiated visit. The mean disease-free survival time after treatment of the secondary event was 72 months (SD, 17 months) in the "own initiative" group and 65 months (SD, 13 months) in the routine follow-up group; this difference was not statistically significant (p = .3). Conclusions. The effectiveness of a 10-year routine follow-up, even in patients with early-stage oral SCC, is very limited. These visits on routine basis can be stopped after 5 years. © 2005 Wiley Periodicals, Inc. Head Neck27: XXX,XXX, 2005 [source] Expression of plasminogen activator inhibitor-1, urokinase receptor and laminin ,-2 chain is an early coordinated event in incipient oral squamous cell carcinomaINTERNATIONAL JOURNAL OF CANCER, Issue 12 2006Pia Lindberg Abstract Cancer cell invasion is facilitated by extracellular matrix degrading proteases such as plasmin. We have studied the expression of plasminogen activator inhibitor-1 (PAI-1) and urokinase receptor (uPAR) together with the ,2-chain of laminin-5 (lam-,2) by immunohistochemistry in 20 cases with incipient oral squamous cell carcinoma (SCC). PAI-1-positive neoplastic cells located at the tip of the putative invasive front of grade 1 (incipient) carcinoma were seen in 16 of the 20 cases (75%), whereas adjacent normal and dysplastic epithelium was PAI-1-negative. Clusters of putative invasive neoplastic cells located in the lamina propria were PAI-1-positive in areas with grade 2 incipient carcinoma as were invasive cancer cells in areas of grade 3,4 invasive carcinoma. uPAR immunoreactivity was strongly expressed in numerous stromal cells in the carcinoma area in all 20 lesions, while a few uPAR-positive stromal cells were found in areas with normal and dysplastic epithelium. uPAR-positive neoplastic cell islands located at the front of the lesions were seen in 15 of the 20 cases. The expression pattern of lam-,2 was very similar to that of PAI-1; however, lam-,2-positive neoplastic cells were only detected in 11 of the 20 cases (55%) in areas of grade 1 incipient carcinoma. Direct comparison of the 3 components revealed colocalization in neoplastic cell islands in both incipient and invasive SCC. Our results suggest that PAI-1 is a novel potential marker of initial invasion in oral SCC, and that the coordinated expression of PAI-1 with uPAR and lam-,2 sustain the features of the early invasive cancer cells. © 2006 Wiley-Liss, Inc. [source] Cyclin D1 overexpression associates with radiosensitivity in oral squamous cell carcinomaINTERNATIONAL JOURNAL OF CANCER, Issue 3 2001Ph.D., Satoru Shintani D.D.S. Abstract Overexpression of cyclin D1, a G1 cell cycle regulator, is often found in many different tumor types, including oral squamous cell carcinomas (SCC). Recent laboratory experiments have demonstrated that cyclin D1 levels can influence radiosensitivity in various cell lines. This study evaluated the relationship between cyclin D1 expression levels and radiosensitivity in nine oral SCC cell lines (HSC2, HSC3, HSC4, SCC15, SCC25, SCC66, SCC111, Ca9-22, and NAN2) and 41 clinical patients with oral SCC who underwent preoperative radiation therapy. Radiosensitivity of the nine oral SCC cell lines differed greatly in their response to radiation, assessed by a standard colony formation assay. Likewise, the expression of cyclin D1 varied, and the magnitude of the cyclin D1 expression correlated with increased tumor radiosensitivity. The similar significant association between the response to preoperative radiation therapy and cyclin D1 overexpression was observed in the oral SCC patients who were treated with preoperative radiation therapy. These results suggest that cyclin D1 expression levels correlate to radiosensitivity and could be used to predict the effectiveness of radiation therapy on oral SCC. © 2001 Wiley-Liss, Inc. [source] Expression of vascular endothelial growth factor-C correlates with the lymphatic microvessel density and the nodal status in oral squamous cell cancerJOURNAL OF ORAL PATHOLOGY & MEDICINE, Issue 8 2003Roland Sedivy Abstract Background:, The cause of preferential metastatic spreading to cervical lymph nodes in oral squamous cell cancer (SCC) is not quite clear. As the density of microvessels may influence the metastatic behaviour, we were interested in how the density of blood/lymphatic microvessels are related to primary SCC and the clinical course of the disease. Methods:, Lymphatic and blood microvessels of 28 patients with oral SCC were identified immunohistochemically by antibodies against podoplanin and CD34, respectively. Lymphatic microvessel density (LVD) and blood microvessel density (MVD), and the expression of VEGF-C were determined. These findings were compared with the long-term clinicopathological data of the patients. Results:, LVD and MVD were significantly higher than in control tissues. The amount of lymphatic microvessels correlated positively with the expression of VEGF-C, the tumour grade, the nodal status and with later appearing metastasis. The latter three parameters, however, did not influence the clinical course of the disease. Conclusions:, VEGF-C expression in oral SCC triggers lymphatic angiogenesis, which may result in a higher risk for cervical lymph node metastasis. The angiogenetic effect of VEGF-C may also favour the onset of late lymphatic and haematogenous metastases. [source] Increase of mast cells and tumor angiogenesis in oral squamous cell carcinomaJOURNAL OF ORAL PATHOLOGY & MEDICINE, Issue 4 2003Anak Iamaroon Abstract Background:, Although mast cells (MCs) have been implicated in promoting angiogenesis in some malignant tumors, especially of the aerodigestive tract, little is known in oral squamous cell carcinoma (SCC). Methods:, A retrospective study was conducted to elaborate upon the correlation between MCs and tumor angiogenesis in 26 cases of oral SCC, six cases of oral pre-malignant dysplasia, 10 cases of oral hyperkeratosis, and six cases of normal oral mucosa by means of immunohistochemical technique. Results:, The MCs in all lesions and normal oral mucosa strongly expressed tryptase. The densities of MCs and microvessels appeared to increase with disease progression. The MC and microvascular counts were significantly higher in oral SCC than in hyperkeratosis and normal oral mucosa (P < 0.05). A significant correlation between MC and microvascular densities was observed in oral SCC (r = 0.5; P = 0.012). Conclusions:, These findings suggest that MCs may upregulate tumor angiogenesis in oral SCC, perhaps via MC tryptase. [source] | ||||||||||